Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work has shown that spleen necrosis virus (SNV) long terminal repeats (LTRs) are associated with Rex/Rex-responsive element-independent expression of bovine leukemia virus RNA and supports the hypothesis that SNV RNA contains a cis-acting element that interacts with cellular Rex-like proteins. To test this hypothesis, the human immunodeficiency virus type 1 (HIV) Rev/RRE-dependent gag gene was used as a reporter to analyze various SNV sequences. Gag enzyme-linked immunosorbent assay and Western blot analyses reveal that HIV Gag production is enhanced at least 20, 000-fold by the 5' SNV LTR in COS, D17, and 293 cells. Furthermore, SNV RU5 in the sense but not the antisense orientation is sufficient to confer Rev/RRE-independent expression onto a cytomegalovirus-gag plasmid. In contrast, the SNV 3' LTR and 3' untranslated sequence between env and the LTR did not support Rev-independent gag expression. Quantitative RNase protection assays indicate that the SNV 5' RNA terminus enhances cytoplasmic accumulation and polysome association of HIV unspliced and spliced transcripts. However, comparison of the absolute amounts of polysomal RNA indicates that polysome association is not sufficient to account for the significant increase in Gag production by the SNV sequences. Our analysis reveals that the SNV 5' RNA terminus contains a unique cis-acting posttranscriptional control element that interacts with hypothetical cellular Rev-like proteins to facilitate HIV RNA transport and efficient translation.
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PMID:The 5' RNA terminus of spleen necrosis virus contains a novel posttranscriptional control element that facilitates human immunodeficiency virus Rev/RRE-independent Gag production. 1023 46

Spontaneous germinal center (GC)-derived B cell lymphomas of SJL mice (RCS) transcribe a 1.8-kb Mtv-29 mRNA under control of the META-env promoter. The encoded vSAg29 stimulates syngeneic Vbeta16(+) CD4(+) T cells, thereby acquiring T cell help necessary for RCS growth. Other strains of B cell lymphoma-prone mice include Mtv29(+) C57L and MA/MyJ, and the Mtv29(-) Mtv7(+)-recombinant inbred strain, SW x J-1. The lymphomas of these mice produce similar mouse mtv-vSAg-encoding mRNA, as characterized by Northern blotting, PCR, and RNase protection. A 1.8-kb mRNA in C57L/J and MA/MyJ lymphomas hybridized with an Mtv29-specific oligonucleotide, whereas SW x J-1 lymphomas produced 1.8-kb transcripts hybridizing with an Mtv7-specific oligonucleotide. Similar META-env-initiated transcripts were absent from LPS-activated B cells from any strain examined but were detected in Peyer's patch RNA from SJL mice. Like typical SJL-derived RCS, all these lymphomas stimulated syngeneic CD4(+) T cells and Vbeta16(+) T hybridoma cells. Immunohistochemical staining of primary tumors showed the presence of peanut agglutinin binding (PNA(+)) highly mitotic lymphoblasts, suggesting their GC derivation. The findings indicate that this novel mRNA for Mtv29 is present in B cell lymphomas from several Mtv29(+) mouse strains. Additionally, this is the first description of the ability of Mtv7 to produce transcripts that are controlled and spliced identically to those of Mtv29 and that are expressed in SW x J-1, I-A(s+), lymphomas that also stimulate Vbeta16(+) T cells. Our results suggest an important role for mouse mtv-vSAgs and Vbeta16 T cell stimulation in the development of GC-derived murine B cell lymphomas.
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PMID:META-controlled env-initiated transcripts encoding superantigens of murine Mtv29 and Mtv7 and their possible role in B cell lymphomagenesis. 1131 79

In order to study the evolution in vivo of human immunodeficiency virus type 1 (HIV-1) in patients with normal clinical evolution, six individuals were selected from a group of 46 patients followed for 1 to 4 years. Patients were selected not by clinical progression characteristics but on the basis of virus genetic variability, as analysed by heteroduplex mobility assay and RNase A mismatch cleavage method. Two patients displayed a homogeneous virus population, two showed very heterogeneous quasispecies and two presented two distinct variants within the virus population. Virus quasispecies were studied by nucleotide sequencing of the C2-fusion domain of the env gene. Virus evolution was approached by analysing the distribution of genetic distances, calculation of divergence and heterogeneity as well as the K(a)/K(s) ratio and by the construction of the phylogenetic trees. Three patients displayed the same tree topology, characterized by the presence of independent clades supported by high bootstrap values, whereas this pattern was not present in the other three patients. In the three patients displaying independent clades, a recombination analysis was carried out between distinct subpopulations and recombinant variants were identified. In one patient of this group, different selective pressures were detected in distinct virus clades, measured by their corresponding K(a)/K(s) ratios, revealing that different evolutionary forces are occurring at the same time within the same patient. These results show that multiple evolutionary patterns can be found in typical HIV-1-infected patients.
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PMID:Different evolutionary patterns are found within human immunodeficiency virus type 1-infected patients. 1156 42

Apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) is a host cytidine deaminase that is packaged into virions and confers resistance to retroviral infection. APOBEC3G deaminates deoxycytidines in minus strand DNA to deoxyuridines, resulting in G to A hypermutation and viral inactivation. Human immunodeficiency virus type 1 (HIV-1) virion infectivity factor counteracts the antiviral activity of APOBEC3G by inducing its proteosomal degradation and preventing virion incorporation. To elucidate the mechanism of viral suppression by APOBEC3G, we developed a sensitive cytidine deamination assay and analyzed APOBEC3G virion incorporation in a series of HIV-1 deletion mutants. Virus-like particles derived from constructs in which pol, env, and most of gag were deleted still contained high levels of cytidine deaminase activity; in addition, coimmunoprecipitation of APOBEC3G and HIV-1 Gag in the presence and absence of RNase A indicated that the two proteins do not interact directly but form an RNase-sensitive complex. Viral particles lacking HIV-1 genomic RNA which were generated from the gag-pol expression constructs pC-Help and pSYNGP packaged APOBEC3G at 30-40% of the wild-type level, indicating that interactions with viral RNA are not necessary for incorporation. In addition, viral particles produced from an nucleocapsid zinc finger mutant contained approximately 1% of the viral genomic RNA but approximately 30% of the cytidine deaminase activity. The reduction in APOBEC3G incorporation was equivalent to the reduction in the total RNA present in the nucleocapsid mutant virions. These results indicate that interactions with viral proteins or viral genomic RNA are not essential for APOBEC3G incorporation and suggest that APOBEC3G interactions with viral and nonviral RNAs that are packaged into viral particles are sufficient for APOBEC3G virion incorporation.
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PMID:Human apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G) is incorporated into HIV-1 virions through interactions with viral and nonviral RNAs. 1521 Jul 4

An insertion of 6.4 kb is present in intron 9 of 60% of the human complement C4 genes, as well as in the C4 genes of a number of Old World primates. This insertion has the typical genomic organization of endogenous retroviruses, with the three major genes gag, pol and env flanked by long terminal repeats (LTRs). This human endogenous retrovirus K [HERV-K(C4)] insertion is in reverse orientation to the C4 coding sequence. Using RT-PCR as well as RNase protection assays, retroviral transcripts could be detected in different human cell lines which were only present in the antisense orientation of the retrovirus. Furthermore, C4 expression as well as intermediate transcripts comprising both HERV-K(C4) and C4 coding sequences was observed in these cells. These findings were confirmed using real-time PCR to quantitate the number of specific mRNA transcripts. Using reporter gene assays, it could be demonstrated that only the 3'LTR exhibits promoter activity, but in the sense orientation of the retrovirus. It has been suggested earlier that expression of C4 could lead to the transcription of a retroviral antisense RNA, which might protect against exogenous retroviral infections. In a previous study, it was shown that the expression of retroviral-like constructs was significantly downregulated in mouse cells transfected with human C4 genes, and that this downregulation was further modulated after IFN-gamma stimulation of C4 expression. In a new series of experiments, we have now confirmed these observations, using human hepatoma cells constitutively expressing C4. A dose-dependent downregulation of up to 45% caused by hybridization of retroviral sense and genomic HERV-K(C4) antisense RNA was observed. The functional 3'LTR promoter, the presence of retroviral antisense RNA transcripts and the functional detection of HERV-K(C4)-specific antisense activity provide strong evidence for a major role of the HERV-K(C4) insertion in the control of gene expression, resulting in a selective advantage favouring the presence of this element in human and primate C4 genes.
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PMID:Detection of retroviral antisense transcripts and promoter activity of the HERV-K(C4) insertion in the MHC class III region. 1530 46


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